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Effect of Chronic L-Dopa or Melatonin Treatments after Dopamine Deafferentation in Rats: Dyskinesia, Motor Performance, and Cytological Analysis
The present study examines the ability of melatonin to protect striatal dopaminergic loss induced by 6-OHDA in a rat model of Parkinson's disease, comparing the results with L-DOPA-treated rats. The drugs were administered orally daily for a month, their therapeutic or dyskinetic effects were a...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scholarly Research Network
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3302121/ https://www.ncbi.nlm.nih.gov/pubmed/22462019 http://dx.doi.org/10.5402/2012/360379 |
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author | Gutierrez-Valdez, Ana Luisa Anaya-Martínez, Verónica Ordoñez-Librado, José Luis García-Ruiz, Ricardo Torres-Esquivel, Carmen Moreno-Rivera, Montserrat Sánchez-Betancourt, Javier Montiel-Flores, Enrique Avila-Costa, Maria Rosa |
author_facet | Gutierrez-Valdez, Ana Luisa Anaya-Martínez, Verónica Ordoñez-Librado, José Luis García-Ruiz, Ricardo Torres-Esquivel, Carmen Moreno-Rivera, Montserrat Sánchez-Betancourt, Javier Montiel-Flores, Enrique Avila-Costa, Maria Rosa |
author_sort | Gutierrez-Valdez, Ana Luisa |
collection | PubMed |
description | The present study examines the ability of melatonin to protect striatal dopaminergic loss induced by 6-OHDA in a rat model of Parkinson's disease, comparing the results with L-DOPA-treated rats. The drugs were administered orally daily for a month, their therapeutic or dyskinetic effects were assessed by means of abnormal involuntary movements (AIMs) and stepping ability. At the cellular level, the response was evaluated using tyrosine hydroxylase immunoreactivity and striatal ultrastructural changes to compare between L-DOPA-induced AIMs and Melatonin-treated rats. Our findings demonstrated that chronic oral administration of Melatonin improved the alterations caused by the neurotoxin 6-OHDA. Melatonin-treated animals perform better in the motor tasks and had no dyskinetic alterations compared to L-DOPA-treated group. At the cellular level, we found that Melatonin-treated rats showed more TH-positive neurons and their striatal ultrastructure was well preserved. Thus, Melatonin is a useful treatment to delay the cellular and behavioral alterations observed in Parkinson's disease. |
format | Online Article Text |
id | pubmed-3302121 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | International Scholarly Research Network |
record_format | MEDLINE/PubMed |
spelling | pubmed-33021212012-03-29 Effect of Chronic L-Dopa or Melatonin Treatments after Dopamine Deafferentation in Rats: Dyskinesia, Motor Performance, and Cytological Analysis Gutierrez-Valdez, Ana Luisa Anaya-Martínez, Verónica Ordoñez-Librado, José Luis García-Ruiz, Ricardo Torres-Esquivel, Carmen Moreno-Rivera, Montserrat Sánchez-Betancourt, Javier Montiel-Flores, Enrique Avila-Costa, Maria Rosa ISRN Neurol Research Article The present study examines the ability of melatonin to protect striatal dopaminergic loss induced by 6-OHDA in a rat model of Parkinson's disease, comparing the results with L-DOPA-treated rats. The drugs were administered orally daily for a month, their therapeutic or dyskinetic effects were assessed by means of abnormal involuntary movements (AIMs) and stepping ability. At the cellular level, the response was evaluated using tyrosine hydroxylase immunoreactivity and striatal ultrastructural changes to compare between L-DOPA-induced AIMs and Melatonin-treated rats. Our findings demonstrated that chronic oral administration of Melatonin improved the alterations caused by the neurotoxin 6-OHDA. Melatonin-treated animals perform better in the motor tasks and had no dyskinetic alterations compared to L-DOPA-treated group. At the cellular level, we found that Melatonin-treated rats showed more TH-positive neurons and their striatal ultrastructure was well preserved. Thus, Melatonin is a useful treatment to delay the cellular and behavioral alterations observed in Parkinson's disease. International Scholarly Research Network 2012-02-01 /pmc/articles/PMC3302121/ /pubmed/22462019 http://dx.doi.org/10.5402/2012/360379 Text en Copyright © 2012 Ana Luisa Gutierrez-Valdez et al. https://creativecommons.org/licenses/by/3.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Gutierrez-Valdez, Ana Luisa Anaya-Martínez, Verónica Ordoñez-Librado, José Luis García-Ruiz, Ricardo Torres-Esquivel, Carmen Moreno-Rivera, Montserrat Sánchez-Betancourt, Javier Montiel-Flores, Enrique Avila-Costa, Maria Rosa Effect of Chronic L-Dopa or Melatonin Treatments after Dopamine Deafferentation in Rats: Dyskinesia, Motor Performance, and Cytological Analysis |
title | Effect of Chronic L-Dopa or Melatonin Treatments after Dopamine Deafferentation in Rats: Dyskinesia, Motor Performance, and Cytological Analysis |
title_full | Effect of Chronic L-Dopa or Melatonin Treatments after Dopamine Deafferentation in Rats: Dyskinesia, Motor Performance, and Cytological Analysis |
title_fullStr | Effect of Chronic L-Dopa or Melatonin Treatments after Dopamine Deafferentation in Rats: Dyskinesia, Motor Performance, and Cytological Analysis |
title_full_unstemmed | Effect of Chronic L-Dopa or Melatonin Treatments after Dopamine Deafferentation in Rats: Dyskinesia, Motor Performance, and Cytological Analysis |
title_short | Effect of Chronic L-Dopa or Melatonin Treatments after Dopamine Deafferentation in Rats: Dyskinesia, Motor Performance, and Cytological Analysis |
title_sort | effect of chronic l-dopa or melatonin treatments after dopamine deafferentation in rats: dyskinesia, motor performance, and cytological analysis |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3302121/ https://www.ncbi.nlm.nih.gov/pubmed/22462019 http://dx.doi.org/10.5402/2012/360379 |
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